The substantial decline in stroke mortality of more than 50% from 1960 through 1990 appears to have been attributable to both primary and secondary prevention. These data suggest that the long decline in stroke mortality and morbidity in Minneapolis-St Paul has plateaued, although improved detection of stroke with computed tomography prevents an unequivocal conclusion.
A registry‐based case‐control study, involving 120 cases (28 males, 92 females) of lung cancer deaths, was conducted in 1985 in the city of Guangzhou to investigate whether lifestyle factors are associated with an increased incidence of lung cancer in never‐smoking individuals. The cases were matched with two control groups which consisted of non‐respiratory‐disease‐related deaths or non‐respiratory‐related cancer deaths. Lifestyle factors assessed in the study include: personal history of nonmalignant respiratory diseases, practice of fresh vegetable consumption, lifetime occupation and occupational exposure histories, exposure to ETS, degree of indoor air pollution, general conditions of home residence, cooking practices and environments, and family history of cancer. Conditional logistic regression analysis demonstrated a negative association between fresh vegetable consumption and lung cancer risk in both sexes, suggesting that vegetables may exert a “protective” effect against lung cancer in humans. In males, elevated risks were found between lung cancer and occupational exposure. In females, indoor air pollution and kitchen environment were associated with risk of lung cancer. No statistically significant association was observed between lung cancer and all other factors examined, including exposure to ETS. A second case‐control study was performed in 1986 to investigate the possible association between spousal smoking and lung cancer deaths. Cases consisted of 75 never‐smoking females and the two control groups consisted of 128 cases of deaths due to non‐tumor diseases, and 126 cases of deaths due to tumors except lung cancer. When cases were matched against “death‐unrelated‐to‐tumor” controls, the odds ratio [OR] for ETS exposure was 1.19, as gauged by whether or not there was ETS exposure; 0.72 and 1.62, when ETS was assessed based on exposure to less than 20 or to 20 or more cigarettes/day. When ETS exposure was measured by “smokingyears”, ORs of 1.39 and 1.17 were obtained based on less than or equal to 30 years of exposure, respectively. Matching cases against “tumor‐other‐than‐lung cancer” controls show the following: OR was 1.00 based or whether or not there was ETS exposure, 0.62 and 1.36, based on exposure to less than 20 or to 20 or more cigarettes/day, and 1.13 and 0.99, based on less than or equal to 30 years of exposure. In all cases, Ors and the calculated 95% confidence interval [CI] indices show that ETS exposure was not significantly associated with female lung cancer deaths, P>0.05. In summary, both case‐control studies suggest no statistically significant association between exposure to ETS and female lung cancer in this Chinese population.
Background: Cervical cancer is one of the most lethal malignancies among women in the world. Every year about 311,365 women die because of cervical cancer. Chemo-resistance is the main reason of the lethal malignancies, and the mechanism of chemo-resistance in cervical cancer still remains largely elusive. Purpose: Previous studies reported that microRNAs played important biological roles in the chemo-resistance in many types of cancers, in the present study we tried to investigate the biological roles of microRNA-218 in chemo-resistance in cervical cancer cells. Results: Real-time PCR results indicated microRNA-218 was downregulated in cisplatin-resistant HeLa/DDP and SiHa/DDP cells compared with the mock HeLa and SiHa cells. CCK-8 assay results showed upregulation of microRNA-218 enhanced the cisplatin sensitivity of cervical cancer cells; while downregulation of microRNA-218 decreased the cisplatin sensitivity of cervical cancer cells. Dual-luciferase assay indicated survivin was a direct target of microRNA-218. Western blotting and PCR results indicated the expression of survivin in HeLa/DDP and SiHa/DDP cells was significantly increased compared with HeLa and SiHa cells. Further study indicated induction of microRNA-218 decreased the expression of survivin while inhibition of microRNA-218 increased the expression of survivin in cervical cancer cells. Cell apoptosis results indicated induction of microRNA-218 induced the cell apoptosis in cervical cancer cells. Conclusion: Our data revealed microRNA-218 enhanced the cisplatin sensitivity in cervical cancer cells through regulation of cell growth and cell apoptosis, which could potentially benefit to the cervical cancer treatment in the future.
Objective: In this study, we aimed to investigate the function of microRNA-373-3p (miR-373-3p) in the pathogenesis of cervical cancer. Methods: Human and mouse cervical cancer cell lines were transfected with miR-373-3p mimic and inhibitor. Cell proliferation and viability were evaluated with Cell Counting Kit-8 (CCK-8) assay and Lactate Dehydrogenase (LDH) assay, respectively. The AKT1-targeting role of miR-373-3p was analyzed by qPCR and Western blot. Finally, a mouse xenograft cervical tumor model was adopted to study the in vivo effect of miR-373-3p on tumor growth and the expression of AKT1. Results: Over-expression of miR-373-3p significantly reduced the proliferation of cervical carcinoma cell line in vitro. In addition, miR-373-3p overexpression also inhibited cervical cancer growth in tumor-bearing mice. Mechanistically, we found that AKT1 gene can be targeted by miR-373-3p. MiR-373-3p mimic decreased the mRNA and protein expression of AKT1, while the miR-373-3p inhibitor increased the level of AKT1 in cervical cancer cells. AKT1 overexpression rescued the proliferation of cervical cancer cells transfected with miR-373-3p. Conclusion: MiR-373-3p can serve as a novel anti-tumor microRNA in cervical cancer by targeting AKT1.
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